The majority of SIDS deaths occur during periods of presumed sleep in infants 2-4 months postnatal age. During this period of time, significant changes occur in the brain centers which are involved in control of sleep, arousal and respiration. Analysis of sleep architecture has revealed subtle changes in the characteristics of the sleep of SIDS victims and in "at-risk" groups compared to control infants. For example, siblings of SIDS victims had longer intervals between rapid eye movement sleep (REMS) epochs during the first month of life and a decreased tendency to enter short waking periods between 2 and 3 months of age. These findings suggest that "at risk" infants may have an increased tendency to remain asleep and/or a relative failure to arouse from sleep. In view of the speculation that failure to arouse from sleep contributes to SIDS, it is essential to understand the central nervous system mechanisms that modify sleep and arousal during development, and the manner in which such modulators of sleep architecture influence respiratory control and arousal. Temperature is a potent modulator of sleep, arousal, and respiration. Although recent studies have underscored the importance of environmental and body temperatures as possible triggers for SIDS, the specific mechanisms by which temperature may lead to SIDS are unknown. In adults, ambient temperature is a powerful modulator of sleep architecture. Thermoregulatory reflexes are also highly sleep-state dependent. Body temperature is regulated at a lower level in non-REMS compared to wakefulness, and thermal control is severely disrupted in REMS. Similarly, respiratory and arousal reflexes are depressed during REMS. However, little information exists on thermoregulatory and respiratory responses during sleep in early development. Considering the abundance of REMS in the immediate postnatal period, it is necessary to quantify the degree to which thermoregulatory and respiratory reflexes are inhibitory during this sleep state, and to assess the interaction of thermal and respiratory stimuli on arousal thresholds during sleep. Our hypothesis is that temperature plays an integral role in the pathogenesis of many SIDS deaths through its influence on sleep distribution, arousal, and control of breathing. We further hypothesize that a period of sleep deprivation followed by a rise in skin temperature could result in prolonged bouts of REMS with concomitant inhibition of respiratory reflexes. We will also determine how changes in sleep structure, respiration, and thermal homeostasis induced by sleep deprivation are modulated by temperature. The use of the rat pup as an animal model offers an opportunity to test all of these hypotheses by examining the interaction of temperature with sleep and breathing in the early postnatal period.